Ringed seal (Pusa hispida) diet on the west coast of Spitsbergen, Svalbard, Norway: during a time of ecosystem change

Global warming is causing Atlantification of water masses and concomitant changes in food webs in the Barents Sea region. To determine whether changes that have been documented at lower trophic levels are impacting the diet of ringed seals (Pusa hispida) gastrointestinal tracts (GITs) from 99 coastal-feeding ringed seals, collected in western Spitsbergen, Svalbard, were analysed via identification of hard-parts. The study animals were shot in spring (n = 30; April–July) or autumn (n = 69; August–October) during four consecutive years (2014–2017). Thirty different prey types were identified, but most seals (55.6%) had consumed between 2 and 4 different types of prey. Polar cod (Boreogadus saida) dominated the diet of the ringed seals in terms of relative biomass (Bi = 60.0%) and frequency of occurrence (FOi = 86.9%), followed by pricklebacks (Stichaeidae; Bi = 23.4%; FOi = 79.8%). Redundancy analysis (RDA) revealed that year was the only significant predictor explaining variance in autumn diet composition (RDA, F3 = 4.96, AIC = − 76.49, p ≤ 0.0050; blubber content and maturity/sex group were not significant). Blue whiting (Micromesistius poutassou) occurred in the diet in small quantities; this Atlantic fish species has not previously been documented in the ringed seals’ diet. Atlantic cod (Gadus morhua) had the highest Bi (9.2%) among Atlantic prey types. However, despite major changes in the last decade in the fish and zooplankton community in western Svalbard, and consumption of a few Atlantic prey types, the ringed seals’ diet in Svalbard continues to be dominated by Arctic prey, especially polar cod.publishedVersio

Swedish LifeWatch ─ a biodiversity infrastructure integrating and reusing data from citizen science, monitoring and research

With continued pressure on biodiversity and ever-growing conflicts with human development, qualified systems for scenario modelling, impact assessment and decision support are urgently needed. Such systems must be able to integrate complex models and information from many sources and do so in a flexible and transparent way. To that end, as well as for other complicated and data-intensive biodiversity research purposes, the concept of LifeWatch has emerged. The idea of LifeWatch is to construct e-infrastructure and virtual laboratories by integrating large data sources, computational capacities, and tools for analysis and modelling in an open, serviceoriented architecture. To be efficient and accurate, a continuous inflow of large quantities of data is essential. However, even with new techniques, government-funded monitoring data and research data will not feed the system with up-to-date species information of sufficient scale and resolution. To fill this void, skilled amateur observers (citizen scientists) can contribute to a very valuable extent. After a preparatory phase, a Swedish LifeWatch (SLW) consortium was initiated in 2011. Swedish LifeWatch developed an infrastructure where all components are accessible through open web services. At the SLW Analysis portal, different formats of species and environmental data can be accessed instantly, and integrated, analysed, visualized and downloaded at selected temporal, spatial or taxonomic scales. Swedish LifeWatch currently provides 46 million species observations from eight different databases, all harmonized according to standardized formats and the Dyntaxa taxonomic backbone database. Almost 40 million of these observations were provided by citizens through the online reporting system named the Species Observation System (SOS) or Artportalen. This paper describes this system, as well as the incentives that make it so successful. The citizen science data in the SOS are accessible, together with data from research and monitoring, in the SLW infrastructure, making the latter a powerful instrument for large-scale data extraction, visualization and analysis

Long-term prognosis of early-onset breast cancer in a population-based cohort with a known BRCA1/2 mutation status.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.All women in the South Sweden Health Care Region with breast cancer diagnosed aged less than 41 during the period between 1990 and 1995 were contacted in 1996 and offered germline mutation analysis of the BRCA1 and BRCA2 genes. Mutation carriers (n = 20) were compared with noncarriers (n = 201) for overall survival (OS) and risk of contralateral breast cancer (CBC). Mutation carriers were younger at diagnosis and more likely to have ER-negative, PgR-negative and grade III tumors. Median follow-up was 19 years. The 5-, 10-, 15-, and 20-year OS were 60, 45, 39, and 39 % for mutation carriers and 82, 70, 59, and 53 % for noncarriers, respectively (5-year log-rank P = 0.013; 10-year P = 0.008; 15-year P = 0.020; and 20-year P = 0.046). In univariable analysis, there was a trend for an inferior OS for mutation carriers (HR 1.8; 95 % CI 1.0-3.3). When stratified for use of (neo)adjuvant chemotherapy, an inferior OS was significant only for the subgroup of patients who did not receive chemotherapy (HR 3.0; 95 % CI 1.2-7.7). In multivarible analysis, BRCA1/2 mutation status was a significant predictor of OS when adjusting for tumor stage, age, and use of chemotherapy, but not when ER status was also included in the model. The 15-year cumulative risk of CBC was 53 % for mutation carriers and 10 % for noncarriers (HR 5.9; 95 % CI 1.9-18.6); among the noncarriers the risks were 5, 22, and 30 % for patients without close relatives having breast cancer, with second-degree relatives having breast cancer, and with firstdegree relatives with breast cancer, respectively. In conclusion, the poor prognosis of young BRCA1/2 mutation carriers with breast cancer is mainly explained by the prevalent occurrence of negative prognostic factors rather than mutation status per se, and can to at least some extent be abrogated by the use of chemotherapy.Skane County Counsil's Research and Development Foundation The Swedish Breast Cancer Association (BRO) BioCAR

Modeling carbon allocation in trees: a search for principles

We review approaches to predicting carbon and nitrogen allocation in forest models in terms of their underlying assumptions and their resulting strengths and limitations. Empirical and allometric methods are easily developed and computationally efficient, but lack the power of evolution-based approaches to explain and predict multifaceted effects of environmental variability and climate change. In evolution-based methods, allocation is usually determined by maximization of a fitness proxy, either in a fixed environment, which we call optimal response (OR) models, or including the feedback of an individual's strategy on its environment (game-theoretical optimization, GTO). Optimal response models can predict allocation in single trees and stands when there is significant competition only for one resource. Game-theoretical optimization can be used to account for additional dimensions of competition, e.g., when strong root competition boosts root allocation at the expense of wood production. However, we demonstrate that an OR model predicts similar allocation to a GTO model under the root-competitive conditions reported in free-air carbon dioxide enrichment (FACE) experiments. The most evolutionarily realistic approach is adaptive dynamics (AD) where the allocation strategy arises from eco-evolutionary dynamics of populations instead of a fitness proxy. We also discuss emerging entropy-based approaches that offer an alternative thermodynamic perspective on allocation, in which fitness proxies are replaced by entropy or entropy production. To help develop allocation models further, the value of wide-ranging datasets, such as FLUXNET, could be greatly enhanced by ancillary measurements of driving variables, such as water and soil nitrogen availability

High risk of in-breast tumor recurrence after BRCA1/2-associated breast cancer.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageThe purpose of the study was to compare breast-conserving therapy (BCT) and mastectomy (M) in BRCA1/2 mutation carriers. Women with invasive breast cancer and a pathogenic mutation in BRCA1 or BRCA2 were included in the study (n = 162). Patients treated with BCT (n = 45) were compared with patients treated with M (n = 118). Endpoints were local recurrence as first recurrence (LR), overall survival (OS), breast cancer death, and distant recurrence. Cumulative incidence was calculated in the presence of competing risks. For calculation of hazard ratios and for multivariable analysis, cause-specific Cox proportional hazards regression was used. Compared to M, BCT was associated with an increased risk of LR in univariable analysis (HR 4.0; 95 % CI 1.6-9.8) and in multivariable analysis adjusting for tumor stage, age, and use of adjuvant chemotherapy (HR 2.9; CI 1.1-7.8). Following M, all local recurrences were seen in the first 5 years after breast cancer diagnosis. Following BCT, the rate of LR continued to be high also after the first 5 years. The cumulative incidence of LR in the BCT group was 15, 25, and 32 % after 5, 10, and 15 years, respectively. There were no significant differences between BCT and M for OS, breast cancer death, or distant recurrence. BRCA1/2 mutation carriers treated with BCT have a high risk of LR, many of which are new primary breast cancers. This must be thoroughly discussed with the patient and is an example of how rapid treatment-focused genetic testing could influence choice of treatment.Regional Ethical Review Board in Lund Skane County Counsil's Research and Development Foundation Swedish Breast Cancer Association (BRO) Swedish Cancer Society BioCAR

High risk of in-breast tumor recurrence after BRCA1/2-associated breast cancer

The purpose of the study was to compare breast-conserving therapy (BCT) and mastectomy (M) in BRCA1/2 mutation carriers. Women with invasive breast cancer and a pathogenic mutation in BRCA1 or BRCA2 were included in the study (n = 162). Patients treated with BCT (n = 45) were compared with patients treated with M (n = 118). Endpoints were local recurrence as first recurrence (LR), overall survival (OS), breast cancer death, and distant recurrence. Cumulative incidence was calculated in the presence of competing risks. For calculation of hazard ratios and for multivariable analysis, cause-specific Cox proportional hazards regression was used. Compared to M, BCT was associated with an increased risk of LR in univariable analysis (HR 4.0; 95 % CI 1.6-9.8) and in multivariable analysis adjusting for tumor stage, age, and use of adjuvant chemotherapy (HR 2.9; CI 1.1-7.8). Following M, all local recurrences were seen in the first 5 years after breast cancer diagnosis. Following BCT, the rate of LR continued to be high also after the first 5 years. The cumulative incidence of LR in the BCT group was 15, 25, and 32 % after 5, 10, and 15 years, respectively. There were no significant differences between BCT and M for OS, breast cancer death, or distant recurrence. BRCA1/2 mutation carriers treated with BCT have a high risk of LR, many of which are new primary breast cancers. This must be thoroughly discussed with the patient and is an example of how rapid treatment-focused genetic testing could influence choice of treatment

Autocatalytic amplification of Alzheimer-associated Aβ42 peptide aggregation in human cerebrospinal fluid

Funder: Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation); doi: https://doi.org/10.13039/501100004063Funder: Alzheimerfonden; doi: https://doi.org/10.13039/501100008599Abstract: Alzheimer’s disease is linked to amyloid β (Aβ) peptide aggregation in the brain, and a detailed understanding of the molecular mechanism of Aβ aggregation may lead to improved diagnostics and therapeutics. While previous studies have been performed in pure buffer, we approach the mechanism in vivo using cerebrospinal fluid (CSF). We investigated the aggregation mechanism of Aβ42 in human CSF through kinetic experiments at several Aβ42 monomer concentrations (0.8–10 µM). The data were subjected to global kinetic analysis and found consistent with an aggregation mechanism involving secondary nucleation of monomers on the fibril surface. A mechanism only including primary nucleation was ruled out. We find that the aggregation process is composed of the same microscopic steps in CSF as in pure buffer, but the rate constant of secondary nucleation is decreased. Most importantly, the autocatalytic amplification of aggregate number through catalysis on the fibril surface is prevalent also in CSF

Discriminatory Analysis of Biochip-Derived Protein Patterns in CSF and Plasma in Neurodegenerative Diseases

The role of biomarkers in neurodegenerative diseases has been emphasized by recent research. Future clinical demands for identifying diseases at an early stage may render them essential. The aim of this pilot study was to test the analytical performance of two multiplex assays of cerebral markers on a well-defined clinical material consisting of patients with various neurodegenerative diseases. We measured 10 analytes in plasma and cerebrospinal fluid (CSF) from 60 patients suffering from Alzheimer's disease (AD), vascular dementia, frontotemporal dementia, dementia with Lewy bodies, or mild cognitive impairment, as well as 20 cognitively healthy controls. We used the Randox biochip-based Evidence Investigator™ system to measure the analytes. We found it possible to measure most analytes in both plasma and CSF, and there were some interesting differences between the diagnostic groups, although with large overlaps. CSF heart-type fatty acid-binding protein was increased in AD. Glial fibrillary acidic protein and neutrophil gelatinase-associated lipocalin in CSF and D-dimer in plasma were elevated in patients with cerebrovascular disease. A multivariate statistical analysis revealed that the pattern of analytes could help to differentiate the conditions, although more studies are required to verify this

Distinct cerebrospinal fluid amyloid β peptide signatures in sporadic and PSEN1 A431E-associated familial Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Alzheimer's disease (AD) is associated with deposition of amyloid β (Aβ) in the brain, which is reflected by low concentration of the Aβ1-42 peptide in the cerebrospinal fluid (CSF). There are at least 15 additional Aβ peptides in human CSF and their relative abundance pattern is thought to reflect the production and degradation of Aβ. Here, we test the hypothesis that AD is characterized by a specific CSF Aβ isoform pattern that is distinct when comparing sporadic AD (SAD) and familial AD (FAD) due to different mechanisms underlying brain amyloid pathology in the two disease groups.</p> <p>Results</p> <p>We measured Aβ isoform concentrations in CSF from 18 patients with SAD, 7 carriers of the FAD-associated presenilin 1 (<it>PSEN1</it>) A431E mutation, 17 healthy controls and 6 patients with depression using immunoprecipitation-mass spectrometry. Low CSF levels of Aβ1-42 and high levels of Aβ1-16 distinguished SAD patients and FAD mutation carriers from healthy controls and depressed patients. SAD and FAD were characterized by similar changes in Aβ1-42 and Aβ1-16, but FAD mutation carriers exhibited very low levels of Aβ1-37, Aβ1-38 and Aβ1-39.</p> <p>Conclusion</p> <p>SAD patients and <it>PSEN1 </it>A431E mutation carriers are characterized by aberrant CSF Aβ isoform patterns that hold clinically relevant diagnostic information. <it>PSEN1 </it>A431E mutation carriers exhibit low levels of Aβ1-37, Aβ1-38 and Aβ1-39; fragments that are normally produced by γ-secretase, suggesting that the <it>PSEN1 </it>A431E mutation modulates γ-secretase cleavage site preference in a disease-promoting manner.</p

Apolipoprotein E Genotype and the Diagnostic Accuracy of Cerebrospinal Fluid Biomarkers for Alzheimer Disease.

Several studies suggest that the apolipoprotein E (APOE) ε4 allele modulates cerebrospinal fluid (CSF) levels of β-amyloid 42 (Aβ42). Whether this effect is secondary to the association of the APOE ε4 allele with cortical Aβ deposition or whether APOE ε4 directly influences CSF levels of Aβ42 independently of Aβ pathology remains unknown